Cite this article: Bhigjee AI, Jeena HC (2014) Bilateral Hemifacial Spasms as a Presenting Manifestation of Multiple Sclerosis: A Case Report. J Neurol Transl Neurosci 2(2): 1043. Central Journal of Neurology & Translational Neuroscience Corresponding author Bhigjee AI, Department of Neurology, The Nelson R Mandela School of Medicine, University of Kwazulu- Natal, Inkosi Albert Luthuli Central Hospital, Private Bag X03, Mayville, 4058, South Africa, Tel: 27- 31-2402359; Fax: 27-31-2402358; Email: Submitted: 09 January 2014 Accepted: 03 February 2014 Published: 13 February 2014 ISSN: 2333-7087 Copyright © 2014 Bhigjee et al. OPEN ACCESS Keywords • Multiple sclerosis • Hemifacial spasm • Bilateral hemifacial Case Report Bilateral Hemifacial Spasms as a Presenting Manifestation of Multiple Sclerosis: A Case Report Ahmed I Bhigjee* and Harshadh C Jeena Department of Neurology, The Nelson R Mandela School of Medicine, University of Kwazulu- Natal, South Africa Abstract Paroxysmal symptoms are common in Multiple Sclerosis. They include tonic spasms, paroxysmal dysarthria, ataxia and Lhermitte’s symptom. A rare manifestation is hemifacial spasm. We present a case of Multiple Sclerosis where the presenting symptom was hemifacial spasm thought to be due to a central area of demyelination. ABBREVIATIONS MS: Multiple Sclerosis; HFS: Hemifacial Spasm INTRODUCTION Paroxysmal symptoms are a characteristic feature of multiple sclerosis (MS). They are distinguished by their acute onset, short duration lasting 10 to 120 seconds and occurring several times a day. The paroxysmal symptoms may occur spontaneously or be triggered by factors such as stress, movement, exercise or hot baths. The nature of the paroxysmal symptoms depends on their site of origin, usually brainstem or spinal cord and may be motor, sensory or visual. Examples include motor symptoms such as tonic spasms, painful tonic contraction of one or more limbs, paroxysmal dysarthria, ataxia, akinesia, hemifacial spasm and myokymia. Sensory disturbances include the Lhermitte’s symptom, trigeminal neuralgia, paroxysmal itching and phosphenes. We describe a male patient whose first presentation of multiple sclerosis was bilateral hemifacial spasms starting at the age of 9 years. CASE PRESENTATION An Asian male first presented in 2009 at the age of 9 years, to his family practitioner with “pulling up” of the left side of his face. There was no preceding illness. He was treated with steroids and the twitching resolved after two weeks. A year later he presented with identical symptoms, but this time he had a preceding flu like illness. The treatment and outcome was similar to the first episode. At the end of 2011 he developed twitching of the right side of the face and impaired balance. He was again treated with steroids but this time the problem did not resolve completely. He was seen in our unit for the first time in June 2012. He also now complained of gait difficulties and fatigue. There were no visual or sensory symptoms. There was no other past history or family history of note. On examination he had normal visual acuity and fundi. The right hemifacial spasm was noted. He had impaired sensation to pinprick and light touch on the right side of the face and the right corneal reflex was depressed. The rest of the cranial nerves were normal. The tone and power in the upper limbs were normal. The legs were spastic with normal power. The right biceps and both supinator jerks were depressed. The knee and ankle jerks were brisk, the abdominal reflexes were absent and both plantar responses were equivocal. He had a right hemisensory impairment to pinprick and light touch. Joint position sense was normal. Coordination was impaired in the lower limbs. Tandem gait was defective. Rhombergism was absent. The following blood tests were normal or negative: full blood count, ESR, urea & electrolytes, liver function tests, anti-nuclear factor, thyroid function tests, immunoglobulins, serum protein electrophoresis, vitamin B12, folate, vitamin D and RPR. The cerebrospinal fluid (CSF) was acellular, had a protein of 0.21 g/l and glucose of 3.4 mmol/litre. Gram and auramine stains were negative. Oligoclonal bands were present in the CSF. The visual evoked responses were normal. Magnetic resonance imaging of brain showed multiple T2 hyperintense lesions in the juxta-cortical areas, periventricular regions, infratentorial areas and in the cervical cord. Several of the supra-tentorial lesions demonstrated contrast enhancement (Figures 1a – d). The pontine lesions may have affected the VII th nerve nucleus or fascicle. This could explain the hemifacial spasm and suggest that the hemifacial spasm was of central region. Special Issue on Multiple Sclerosis